Co-regulation of p16INK4A and migratory genes in culture conditions that lead to premature senescence in human keratinocytes.

ABSTRACT: Cellular stasis, also known as telomere-independent senescence, prevents many epithelial cells from becoming immortalized by telomerase alone. As human keratinocytes age in culture, protein levels of the tumor suppressor p16INK4a continue to increase, resulting in growth arrest independent of telomere length. Differences in culture conditions have been shown to modulate both p16INK4a expression and replicative capacity of human keratinocytes; however, the mechanism of p16INK4a induction under these conditions is unknown. Using multiple primary keratinocyte cell strains, we verified a delay in p16INK4a induction and an extended lifespan of human keratinocytes when grown in co-culture with post-mitotic fibroblast feeder cells as compared with keratinocytes grown on tissue culture plastic alo

SUBMITTER: Darbro BW 

PROVIDER: S-EPMC2020850 | biostudies-literature | 2005 Sep

REPOSITORIES: biostudies-literature